Cell action mechanism of tranilast — Effect on the expression of HLA-class II antigen

Kawano, Yutaka; Noma, Takeshi

doi:10.1016/0192-0561(93)90063-5

Cited by 10 publications

(3 citation statements)

References 32 publications

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“…In addition, it also inhibits the surface expression of VCAM-1 in fibroblasts [19,24], expression of ICAM-1 from monocytes [25], release of IL-2 and IL-1␤ from monocytes and macrophages [26], release of TGF-␤1 from fibroblasts [17,26] also from mast cells and basophils [27], MMP-2 and -9 production from fibroblasts and neutrophils [28,29] as well as INF-␥ and TNF-␣ production [7]. Furthermore, the expression of HLA-DR and -DQ antigens on macrophages was significantly suppressed by treatment with tranilast [30]. Tranilast has also been shown to suppress oxygen free radical production from human neutrophils [31].…”

Section: Allergic Diseases Inflammatory Diseases and Immunitymentioning

confidence: 93%

Tranilast: A review of its therapeutic applications

Darakhshan

Pour

2015

Pharmacological Research

247

225

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Section: Allergic Diseases Inflammatory Diseases and Immunitymentioning

confidence: 93%

Tranilast: A review of its therapeutic applications

Darakhshan

Pour

2015

Pharmacological Research

247

225

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“…Tranilast possesses immunomodulatory activities (Kawano and Noma 1993;Matsumura et al 1999); it inhibits the release of cytokines and chemical mediators from various cells, including macrophages and fibroblasts (Qi et al 2006). It inhibits collagen synthesis in fibroblasts, vascular smooth muscle cells and macrophages (Suzawa et al 1992b;Isaji et al 1998;Soma et al 2002).…”

Section: Introductionmentioning

confidence: 97%

Tranilast ameliorates impaired hepatic functions in Schistosoma mansoni-infected mice

Said

Elkashef

et al. 2012

Inflammopharmacol

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The ability of tranilast, a mast cell stabilizer and anti-transforming growth factor(β) (TGF(β)) to improve impaired hepatic functions in Schistosoma mansoni (S. mansoni)-infected mice, was investigated, providing the first evidence on the ability of tranilast to improve hepatic impairment due to schistosomal infection. Tranilast had significant beneficial effects against progression of hepatic fibrosis in S. mansoni-infected mice treated with praziquantel and those untreated. Different aspects of drug activity were investigated. Its effect on serum liver functions was evaluated by estimating: alanine aminotransferase, aspartate aminotransferase, total bilirubin, alkaline phosphatase and albumin. Its effect on the extent of liver fibrosis, through estimation of hepatic hydroxyproline and hepatic collagen content in liver hydrolysates, was also evaluated. Also, the expression of profibrogenic mediators, such as serum TGF(β1), was estimated. Finally, the effect on S. mansoni infection itself was studied, via histopathological examination of liver specimens stained with both hematoxylin-eosin and Masson's trichome stains. Tranilast ameliorated the harmful effects of S. mansoni infection on the liver. Such action was manifested in its significant ability to improve impaired hepatic functions, reduce histopathological changes, lower hepatic collagen content and finally reduce serum TGF(β1) levels. The beneficial effect of tranilast may be in part due to its ability to reduce the production of profibrogenic mediators in the infected animals by improving the host immune response or by interfering with critical steps in the fibrogenic cascade.

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“…The inhibitory effects of tranilast on collagen accumulation, proliferation and migration of different cell types may be attributed to antagonizing TGF‐β (Fukuyama et al ., 1996; Miyazawa et al ., 1995). The suppressive effects on fibrosis may involve the inhibition of activated macrophages known to release NO (Kawano & Noma, 1993; Mori et al ., 1995; Suzawa et al ., 1992). On the other hand, there are lines of evidence that tranilast may be a positive regulator of iNOS expression and activity in vascular smooth muscle cells and rat mesangial cells (Hishikawa et al ., 1996).…”

Section: Introductionmentioning

confidence: 99%

N‐[3,4‐dimethoxycinnamoyl]‐anthranilic acid (tranilast) suppresses microglial inducible nitric oxide synthase (iNOS) expression and activity induced by interferon‐γ (IFN‐γ)

Platten

Wick

Wischhusen

et al. 2001

British J Pharmacology

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1 Microglial cells up-regulate inducible nitric oxide synthase (iNOS) expression in response to various pro-in¯ammatory stimuli including interferon-g (IFN-g), allowing for the release of nitric oxide (NO). Tranilast (N-[3,4-dimethoxycinnamoyl]-anthranilic acid) is an antiallergic compound with suppressive e ects on the activation of monocytes. 2 Here, we show that N9 murine microglial cells express iNOS mRNA and protein and release nitric oxide into the culture medium in response to IFN-g (200 u ml 71 ) as measured by Northern and Western blot analyses and Griess assay. 3 Exposure to non-toxic doses of tranilast (30 ± 300 mM) leads to a concentration-dependent inhibition of IFN-g-induced (200 u ml 71 ) iNOS mRNA and protein expression. This is paralleled by a suppression of NO-release into the cell culture medium. 4 Inhibition of IFN-g-induced iNOS mRNA expression by tranilast is paralleled by an inhibition of nuclear factor-kB (NF-kB) activation and phosphorylation of inhibitory kB (IkB) as determined by Western blot analyses and NF-kB reporter gene assay. 5 These results suggest that tranilast-mediated suppression of microglial iNOS activity induced by IFN-g involves the inhibition of NF-kB-dependent iNOS mRNA expression.

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Cell action mechanism of tranilast — Effect on the expression of HLA-class II antigen

Cited by 10 publications

References 32 publications

Tranilast: A review of its therapeutic applications

Tranilast: A review of its therapeutic applications

Tranilast ameliorates impaired hepatic functions in Schistosoma mansoni-infected mice

N‐[3,4‐dimethoxycinnamoyl]‐anthranilic acid (tranilast) suppresses microglial inducible nitric oxide synthase (iNOS) expression and activity induced by interferon‐γ (IFN‐γ)

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